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Deficiency of IL-22 contributes to a chronic inflammatory disease: pathogenetic mechanisms in acne inversa Wolk K; Warszawska K; Hoeflich C; Witte E; Schneider-Burrus S; Witte K; Kunz S; Buss A; Roewert HJ; Krause M; Lukowsky A; Volk HD; Sterry W; Sabat RJ Immunol 2011[Jan]; 186 (2): 1228-39Overexpression of the T cell cytokine IL-22 is linked to the development of some chronic diseases, but little is known about IL-22 deficiency in humans. As demonstrated in this study, acne inversa (AI; also designated as Hidradenitis suppurativa) lesions show a relative deficiency of IL-22 and IL-20, but not of IL-17A, IL-26, IFN-gamma, IL-24, or IL-1beta. Moreover, AI lesions had reduced expression of membranous IL-22 and IL-20 receptors and increased expression of the natural IL-22 inhibitor, IL-22 binding protein. AI is a chronic inflammatory skin disease with prevalence up to 4% of the population and in which cutaneous bacterial persistence represents an important pathogenetic factor. Accordingly, we also found a relative deficiency of antimicrobial proteins (AMPs) in AI lesions and a positive correlation between lesional IL-22 and IL-20 versus AMP levels. IL-22, like its tissue cell downstream mediator IL-20, upregulated AMPs in reconstituted human epidermis and was critical for increased AMP levels under inflammatory conditions. The relative IL-22 deficiency in AI was not linked to lesional T cell numbers or Th22/Th1/Th17 subset markers and -inducing cytokines. However, IL-10 was highly expressed in AI lesions and correlated negatively with IL-22 expression. Moreover, IL-10 inhibited IL-22 but not IL-17 production in vitro. The IL-10 overexpression, in turn, was not associated with an elevated presence of regulatory T cells but with the enhanced presence of an IL-10-inducing cytokine. We conclude that IL-22 deficiency may contribute to the pathogenesis of certain chronic disorders as postulated in this paper for AI.|Adolescent[MESH]|Adult[MESH]|Aged[MESH]|Animals[MESH]|Antimicrobial Cationic Peptides/deficiency/physiology[MESH]|Cells, Cultured[MESH]|Chronic Disease[MESH]|Cytokines/biosynthesis/deficiency[MESH]|Female[MESH]|Hidradenitis Suppurativa/*immunology/metabolism/*pathology[MESH]|Humans[MESH]|Inflammation Mediators/metabolism/*physiology[MESH]|Inflammation/immunology/metabolism/pathology[MESH]|Interleukin-22[MESH]|Interleukins/*deficiency/genetics/physiology[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred BALB C[MESH]|Middle Aged[MESH]|Up-Regulation/immunology[MESH]|Young Adult[MESH] |
